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417 results on '"Pannicke, Thomas"'

2. Effects of IP3R2 Receptor Deletion in the Ischemic Mouse Retina

Author

Wagner, Lysann, Pannicke, Thomas, Frommherz, Ina, Sauer, Katja, Chen, Ju, and Grosche, Antje

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Eye Disease and Disorders of Vision, Neurosciences, 2.1 Biological and endogenous factors, Aetiology, Animals, Cell Count, Ependymoglial Cells, Gliosis, Inositol 1, 4, 5-Trisphosphate Receptors, Ischemia, Mice, Knockout, Neurons, Retina, P2Y(1), IP(3)R2, Glia, Mouse, IP3R2, P2Y1, Biological Sciences, Medical and Health Sciences, Neurology & Neurosurgery
Abstract

Glial cells in the diseased nervous system undergo a process known as reactive gliosis. Gliosis of retinal Müller glial cells is characterized by an upregulation of glial fibrillary acidic protein and frequently by a reduction of inward K(+) current amplitudes. Purinergic signaling is assumed to be involved in gliotic processes. As previously shown, lack of the nucleotide receptor P2Y1 leads to an altered regulation of K(+) currents in Müller cells of the ischemic retina. Here, we asked first whether this effect is mediated by the IP3 receptor subtype 2 (IP3R2) known as the major downstream signaling target of P2Y1 in Müller cells. The second question was whether lack of IP3R2 affects neuronal survival in the control and ischemic retina. Ischemia was induced in wild type and IP3R2-deficient (IP 3 R2 (-/-)) mice by transient elevation of the intraocular pressure. Immunostaining and TUNEL labelling were used to quantify neuronal cell loss. The downregulation of inward K(+) currents in Müller cells from ischemic IP 3 R2 (-/-) retinae was less strong than in wild type animals. The reduction of the number of cells in the ganglion cell layer and of calretinin- and calbindin-positive cells 7 days after ischemia was similar in wild type and IP 3 R2 (-/-) mice. However, IP3R2 deficiency led to an increased number of TUNEL-positive cells in the outer nuclear layer at 1 day and to an enhanced postischemic loss of photoreceptors 7 days after ischemia. This implies that IP3R2 is involved in some but not all aspects of signaling in Müller cells after an ischemic insult.

Published
2016

8. Development and Functional Characterization of Fetal Lung Organoids

Author

Laube, Mandy, Pietsch, Soeren, Pannicke, Thomas, Thome, Ulrich H., Fabian, Claire, and Publica

Subjects
lung, 3D culture, organoids, patch clamp, fetal development, model system, 3D culture, Medicine (General), organoid, fetal development, Lunge, General Medicine, respiratory system, patch-clamp recordings, patch clamp, lung, R5-920, Medicine, ddc:610, model system, organoids, Original Research
Abstract

Preterm infants frequently suffer from pulmonary complications due to a physiological and structural lung immaturity resulting in significant morbidity and mortality. Novel in vitro and in vivo models are required to study the underlying mechanisms of late lung maturation and to facilitate the development of new therapeutic strategies. Organoids recapitulate essential aspects of structural organization and possibly organ function, and can be used to model developmental and disease processes. We aimed at generating fetal lung organoids (LOs) and to functionally characterize this in vitro model in comparison to primary lung epithelial cells and lung explants ex vivo. LOs were generated with alveolar and endothelial cells from fetal rat lung tissue, using a Matrigel-gradient and air-liquid-interface culture conditions. Immunocytochemical analysis showed that the LOs consisted of polarized epithelial cell adhesion molecule (EpCAM)-positive cells with the apical membrane compartment facing the organoid lumen. Expression of the alveolar type 2 cell marker, RT2-70, and the Club cell marker, CC-10, were observed. Na+ transporter and surfactant protein mRNA expression were detected in the LOs. First time patch clamp analyses demonstrated the presence of several ion channels with specific electrophysiological properties, comparable to vital lung slices. Furthermore, the responsiveness of LOs to glucocorticoids was demonstrated. Finally, maturation of LOs induced by mesenchymal stem cells confirmed the convenience of the model to test and establish novel therapeutic strategies. The results showed that fetal LOs replicate key biological lung functions essential for lung maturation and therefore constitute a suitable in vitro model system to study lung development and related diseases.

Published
2021

30. Glial cells in (patho)physiology

Author

Parpura, Vladimir, Heneka, Michael T., Montana, Vedrana, Oliet, Stéphane H. R., Schousboe, Arne, Haydon, Philip G., Stout, Randy F., Spray, David C., Reichenbach, Andreas, Pannicke, Thomas, Pekny, Milos, Pekna, Marcela, Zorec, Robert, and Verkhratsky, Alexei

Published
2012
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34. Suppression of SNARE‐dependent exocytosis in retinal glial cells and its effect on ischemia‐induced neurodegeneration

Author

Wagner, Lysann, Pannicke, Thomas, Rupprecht, Vanessa, Frommherz, Ina, Volz, Cornelia, Illes, Peter, Hirrlinger, Johannes, Jägle, Herbert, Egger, Veronica, Haydon, Philip G., Pfrieger, Frank W., and Grosche, Antje

Subjects
Retinal Ganglion Cells, Vascular Endothelial Growth Factor A, retina, Protein Kinase C-alpha, Light, Ependymoglial Cells, Intermediate Filaments, Glutamic Acid, glutamate, Mice, Transgenic, ischemia, Exocytosis, Mice, Receptors, Purinergic P2Y1, Glial Fibrillary Acidic Protein, Animals, Research Articles, gliotransmitter, Müller cell, Calcium-Binding Proteins, Microfilament Proteins, Disease Models, Animal, nervous system, Doxycycline, Nerve Degeneration, SNARE Proteins, Research Article
Abstract

Nervous tissue is characterized by a tight structural association between glial cells and neurons. It is well known that glial cells support neuronal functions, but their role under pathologic conditions is less well understood. Here, we addressed this question in vivo using an experimental model of retinal ischemia and transgenic mice for glia‐specific inhibition of soluble N‐ethylmaleimide‐sensitive factor attachment protein receptor (SNARE)‐dependent exocytosis. Transgene expression reduced glutamate, but not ATP release from single Müller cells, impaired glial volume regulation under normal conditions and reduced neuronal dysfunction and death in the inner retina during the early stages of ischemia. Our study reveals that the SNARE‐dependent exocytosis in glial cells contributes to neurotoxicity during ischemia in vivo and suggests glial exocytosis as a target for therapeutic approaches.

Published
2017

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